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Updated: Jan 21, 2026

Production and Detection of Reactive Oxygen Species ROS in Cancers
Published on: November 21, 2011
Anatomically specific reactive oxygen species production participates in Marfan syndrome aneurysm formation
Fabian Emrich1,2, Kiril Penov1,2, Mamoru Arakawa1,3
1Department of Cardiothoracic Surgery, Stanford University, Stanford, California.
Abstract:
Marfan syndrome (MFS) is a connective tissue disorder that results in aortic root aneurysm formation. Reactive oxygen species (ROS) seem to play a role in aortic wall remodelling in MFS, although the mechanism remains unknown. MFS Fbn1C1039G/+ mouse root/ascending (AS) and descending (DES) aortic samples were examined using DHE staining, lucigenin-enhanced chemiluminescence (LGCL), Verhoeff's elastin-Van Gieson staining (elastin breakdown) and in situ zymography for protease activity. Fbn1C1039G/+ AS- or DES-derived smooth muscle cells (SMC) were treated with anti-TGF-β antibody, angiotensin II (AngII), anti-TGF-β antibody + AngII, or isotype control. ROS were detected during early aneurysm formation in the Fbn1C1039G/+ AS aorta, but absent in normal-sized DES aorta. Fbn1C1039G/+ mice treated with the unspecific NADPH oxidase inhibitor, apocynin reduced AS aneurysm formation, with attenuated elastin fragmentation. In situ zymography revealed apocynin treatment decreased protease activity. In vitro SMC studies showed Fbn1C1039G/+ -derived AS SMC had increased NADPH activity compared to DES-derived SMC. AS SMC NADPH activity increased with AngII treatment and appeared TGF-β dependent. In conclusion, ROS play a role in MFS aneurysm development and correspond anatomically with aneurysmal aortic segments. ROS inhibition via apocynin treatment attenuates MFS aneurysm progression. AngII enhances ROS production in MFS AS SMCs and is likely TGF-β dependent.
Insights
Reactive oxygen species (ROS) contribute to aortic aneurysm development in Marfan syndrome (MFS). Inhibiting ROS with apocynin reduced aneurysm growth and elastin breakdown in MFS mice.
Area of Science:
- Cardiovascular Biology
- Connective Tissue Disorders
- Molecular Medicine
Background:
- Marfan syndrome (MFS) is a genetic disorder affecting connective tissue, leading to aortic root aneurysm.
- The precise mechanism by which reactive oxygen species (ROS) contribute to aortic wall remodeling in MFS is not fully understood.
Purpose of the Study:
- To investigate the role of ROS in the pathogenesis of aortic aneurysms in a mouse model of Marfan syndrome.
- To explore the potential therapeutic effect of ROS inhibition on aneurysm progression.
Main Methods:
- Analysis of aortic tissues from Marfan syndrome (Fbn1C1039G/+) and control mice using DHE staining, lucigenin-enhanced chemiluminescence (LGCL), and elastin Van-Gieson staining.
- In situ zymography to assess protease activity and in vitro studies on smooth muscle cells (SMCs) treated with TGF-β antibody and angiotensin II (AngII).
Main Results:
- ROS were detected in the ascending aorta of MFS mice during early aneurysm formation.
- Treatment with apocynin, a NADPH oxidase inhibitor, reduced aneurysm formation and elastin fragmentation in MFS mice.
- Angiotensin II (AngII) increased ROS production in MFS aortic SMCs in a TGF-β-dependent manner.
Conclusions:
- ROS play a significant role in the development and progression of aortic aneurysms in Marfan syndrome.
- Inhibition of ROS, for example, via apocynin, can attenuate aneurysm development.
- Angiotensin II contributes to ROS production in MFS aortic smooth muscle cells, suggesting a potential therapeutic target.
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